title: Medical management of compromised brain oxygen in patients with severe traumatic brain injury.
abstract: BACKGROUND
  Brain tissue oxygen (PbtO(2)) monitoring is used in severe traumatic brain injury (TBI) patients. How brain reduced PbtO(2) should be treated and its response to treatment is not clearly defined. We examined which medical therapies restore normal PbtO(2) in TBI patients.
  
  
  METHODS
  Forty-nine (mean age 40 ± 19 years) patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to a University-affiliated, Level I trauma center who had at least one episode of compromised brain oxygen (PbtO(2) <25 mmHg for >10 min), were retrospectively identified from a prospective observational cohort study. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO(2) were monitored continuously. Episodes of compromised PbtO(2) and brain hypoxia (PbtO(2) <15 mmHg for >10 min) and the medical interventions that improved PbtO(2) were identified.
  
  
  RESULTS
  Five hundred and sixty-four episodes of compromised PbtO2 were identified from 260 days of PbtO2 monitoring. Medical management used in a "cause-directed" manner successfully reversed 72% of the episodes of compromised PbtO(2), defined as restoration of a "normal" PbtO(2) (i.e. ≥ 25 mmHg). Ventilator manipulation, CPP augmentation, and sedation were the most frequent interventions. Increasing FiO(2) restored PbtO(2) 80% of the time. CPP augmentation and sedation were effective in 73 and 66% of episodes of compromised brain oxygen, respectively. ICP reduction using mannitol was effective in 73% of treated episodes, though was used only when PbtO(2) was compromised in the setting of elevated ICP. Successful medical treatment of brain hypoxia was associated with decreased mortality. Survivors (n = 38) had a 71% rate of response to treatment and non-survivors (n = 11) had a 44% rate of response (P = 0.01).
  
  
  CONCLUSIONS
  Reduced PbtO(2) may occur in TBI patients despite efforts to maintain CPP. Medical interventions other than those to treat ICP and CPP can improve PbtO(2). This may increase the number of therapies for severe TBI in the ICU.
authors.affiliation: Department of Neurosurgery, University of Pennsylvania, 3 Silverstein Pavilion, 3400 Spruce Street, Philadelphia, PA 19104, USA. Leif-Erik.Bohman@uphs.upenn.edu
authors.forename: Leif-Erik
authors.initials: LE
authors.lastname: Bohman
authors.forename: Gregory G
authors.initials: GG
authors.lastname: Heuer
authors.forename: Lukascz
authors.initials: L
authors.lastname: Macyszyn
authors.forename: Eileen
authors.initials: E
authors.lastname: Maloney-Wilensky
authors.forename: Suzanne
authors.initials: S
authors.lastname: Frangos
authors.forename: Peter D
authors.initials: PD
authors.lastname: Le Roux
authors.forename: Andrew
authors.initials: A
authors.lastname: Kofke
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Levine
authors.forename: Michael F
authors.initials: MF
authors.lastname: Stiefel
mesh_terms: D000328:Adult; D000368:Aged; D000698:Analgesia; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000098:blood supply; D001930:Brain Injuries / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D003131:Combined Modality Therapy; D016292:Procedural Sedation; D003399:Craniotomy; D003422:Critical Care / Q000379:methods*; D019299:Decompression, Surgical; D004234:Diuretics, Osmotic / Q000008:administration & dosage; D005260:Female; D005440:Fluid Therapy; D015600:Glasgow Coma Scale; D017052:Hospital Mortality; D006801:Humans; D002534:Hypoxia, Brain / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D008353:Mannitol / Q000008:administration & dosage; D008875:Middle Aged; D056888:Patient Positioning; D010656:Phenylephrine / Q000008:administration & dosage; D012121:Respiration, Artificial; D012189:Retrospective Studies; D015996:Survival Rate; D055815:Young Adult
chemical_list: D004234:Diuretics, Osmotic; D010656:Phenylephrine; D008353:Mannitol